Gut dysbiosis as a protective adaptation in certain circumstances?
This idea runs contrary to what I thought I understood about gut health, but there are some data to back it up:
The following study showed that pro-inflammatory changes in gut flora WERE NECESSARY to prevent metabolic dysfunction in obese rats:
To understand the biology behind this and for a great overview of the study, you can listen to this podcast by Chris Masterjohn PhD. here is an excerpt:
Basically, visceral adipose tissue requires inflammation to undergo remodelling so that it can store more fat. When it can no longer expand, metabolic dysfunction/syndrome ensues. The inflammation which helps the adipose tissue to remodel (and essentially prevents metabolic syndrome) come from the proinflammatory gut microbiome. Hence, the "dysbiosis" appears to be a protective adaptation, and so is the chronic inflammation for a short period of time.
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I was reminded of Gerald Pollack's work on water and Stephanie Senneff's work on cholesterol sulfate and her various papers on atherosclerosis and cardiovascular disease pathophysiology. The recent work in this area shows that blood flow and lymph flow are potentially facilitated by proteins/molecules located on the surface of the capillary wall structuring the water on the surface of the capillaries, to create a "streaming potential" which can effectively propel negatively charged red blood cells though the vasculature.
Senneff has detailed the critical role of sulfated glycosaminoglycans in this process, and a lack of sulfate could potentially contribute to multiple pathologies we see today, especially cardiovascular related.
Here is a great article she wrote for the WAPF detailing the information of cholesterol sulfate, and here is one of her papers for the more technically minded.
A brief summary provided in the article:
Senneff explains that a certain bacterial species (C.pneumoniae) are commonly found in the atheroma, and that they are the only known species to be able to supply heparan sulfate to the host cells!:
Senneff theorises that the body may specifically select for this bacteria to populate the site of pathology to supply sulfate. In other words, the human body is working together in a mutually beneficial relationship with this specific bacteria. Contrary to the 'pathogenic infection' theory of the atheroma development, she suggests that it is protective and is perhaps evidence of the innate intelligence of the human-microbiome system.
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So we have two interesting pieces of information here:
1. The body appears to facilitate passage of certain bacteria into the blood-stream (C. Pneumoniae) as a last ditch attempt to replenish a deficient resource (in this case, sulfate).
2. Dysbiosis/pro-inflammatory changes to the microbiome appear to be selected for by obese rats to prevent metabolic syndrome. Dysbiosis=helpful
It is starting to look like the body has some control over the microbiome, or is in communication with it at least (well duhh?)
So this left me thinking about chronic digestive issues, dysbiosis, and small intestinal bacterial overgrowth.
WHY do these problems just keep recurring in so many people who appear to have exhausted every avenue? This is a common issue that practitioners face, and Chris Kresser recently did a podcast on it basically admitting that he is unable to work it out, even after like a decade attempting treating it. It is very, very common for SIBO to return shortly after treatments in some people. Additionally, why do 95% of autistic children have rampant Clostridia overgrowth in their gut (according to great plains lab)?
How might this all tie in together and relate to Senneff's work on sulfate?.........
This idea runs contrary to what I thought I understood about gut health, but there are some data to back it up:
The following study showed that pro-inflammatory changes in gut flora WERE NECESSARY to prevent metabolic dysfunction in obese rats:
To understand the biology behind this and for a great overview of the study, you can listen to this podcast by Chris Masterjohn PhD. here is an excerpt:
Basically, visceral adipose tissue requires inflammation to undergo remodelling so that it can store more fat. When it can no longer expand, metabolic dysfunction/syndrome ensues. The inflammation which helps the adipose tissue to remodel (and essentially prevents metabolic syndrome) come from the proinflammatory gut microbiome. Hence, the "dysbiosis" appears to be a protective adaptation, and so is the chronic inflammation for a short period of time.
_____________________________________________________________________________________________________________________
I was reminded of Gerald Pollack's work on water and Stephanie Senneff's work on cholesterol sulfate and her various papers on atherosclerosis and cardiovascular disease pathophysiology. The recent work in this area shows that blood flow and lymph flow are potentially facilitated by proteins/molecules located on the surface of the capillary wall structuring the water on the surface of the capillaries, to create a "streaming potential" which can effectively propel negatively charged red blood cells though the vasculature.
Senneff has detailed the critical role of sulfated glycosaminoglycans in this process, and a lack of sulfate could potentially contribute to multiple pathologies we see today, especially cardiovascular related.
Here is a great article she wrote for the WAPF detailing the information of cholesterol sulfate, and here is one of her papers for the more technically minded.
A brief summary provided in the article:
Senneff explains that a certain bacterial species (C.pneumoniae) are commonly found in the atheroma, and that they are the only known species to be able to supply heparan sulfate to the host cells!:
Senneff theorises that the body may specifically select for this bacteria to populate the site of pathology to supply sulfate. In other words, the human body is working together in a mutually beneficial relationship with this specific bacteria. Contrary to the 'pathogenic infection' theory of the atheroma development, she suggests that it is protective and is perhaps evidence of the innate intelligence of the human-microbiome system.
_____________________________________________________________________________________________________________________
So we have two interesting pieces of information here:
1. The body appears to facilitate passage of certain bacteria into the blood-stream (C. Pneumoniae) as a last ditch attempt to replenish a deficient resource (in this case, sulfate).
2. Dysbiosis/pro-inflammatory changes to the microbiome appear to be selected for by obese rats to prevent metabolic syndrome. Dysbiosis=helpful
It is starting to look like the body has some control over the microbiome, or is in communication with it at least (well duhh?)
So this left me thinking about chronic digestive issues, dysbiosis, and small intestinal bacterial overgrowth.
WHY do these problems just keep recurring in so many people who appear to have exhausted every avenue? This is a common issue that practitioners face, and Chris Kresser recently did a podcast on it basically admitting that he is unable to work it out, even after like a decade attempting treating it. It is very, very common for SIBO to return shortly after treatments in some people. Additionally, why do 95% of autistic children have rampant Clostridia overgrowth in their gut (according to great plains lab)?
How might this all tie in together and relate to Senneff's work on sulfate?.........
